A developmentally-sensitive mechanism underlying the escalation of adolescent social anxiety

青少年社交焦虑升级的发育敏感机制

• 批准号: 10707188
• 负责人: George Arthur Buzzell
• 金额: $ 68.66万
• 依托单位: FLORIDA INTERNATIONAL UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2022
• 资助国家: 美国
• 起止时间: 2022-09-20 至 2027-06-30
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10707188
• 关键词: 15 year old; Acceleration; Address; Adolescence; Adolescent; Adolescent Development; Affect; Age; Anxiety; Anxiety Disorders; Back; Behavior; Biological Markers; Brain; Chronic; Code; Data; Detection; Development; Disease; Electroencephalography; Ensure; Evaluation; Exhibits; Feedback; Feeds; Female; Female Adolescents; Fright; Future; Goals; Impairment; Intervention; Investigational Therapies; Lateral; Lead; Link; Longitudinal Studies; Measures; Medial; Mediating; Methods; Modeling; National Institute of Mental Health; Neurocognitive; Participant; Pathway interactions; Patient Self-Report; Performance; Play; Population; Positioning Attribute; Prevention; Psychopathology; Puberty; Risk; Role; Self-Examination; Social Anxiety Disorder; Social Development; Social Environment; Social Interaction; System; Testing; Theoretical model; Therapeutic; Time; Translating; Work; anxiety symptoms; anxious behavior; bench to bedside; brain based; cognitive control; early adolescence; frontal lobe; improved; male; neural; new therapeutic target; novel; peer; predictive modeling; psychologic; recruit; response; self-reported anxiety; social; social anxiety; social cognition; social interventions; sociodemographics; tool; treatment response

Abstract Social anxiety disorder (SAD) is a chronic, impairing condition that typically emerges during adolescence and affects about 10% of the population. Treatment response rates for SAD are markedly lower than for other anxiety disorders, thus presenting an urgent need to identify novel therapeutic targets that can inform new interventions for this difficult-to-treat disorder. We propose to address this need by testing a developmentally-informed, mechanistic model of the escalation of impairing social anxiety symptoms (SA) in early-to-mid adolescence; our model centers on Fear of Negative Evaluation (FNE) and Hypervigilance for Errors in the presence of peers, with a focus on frontal brain oscillations as central to this escalation. Adolescence represents a sensitive period for the development of social cognition and cognitive control. At the psychological level, social fears and FNE exhibit normative increases across adolescence, given the increasing importance of peers during this developmental window. At the neural level, frontal brain systems underlying social cognition and cognitive control exhibit protracted development across adolescence, including development of the frontal cortex and associated 4-8 Hz “theta” oscillations causally implicated in cognitive control. Our central hypothesis is that adolescent increases in FNE, alongside development of the frontal cortex, create a maladaptive feedback loop: adolescents become Hypervigilant to Errors in social settings, further increasing FNE, and ultimately, impairing SA. Our model predicts (Aim 1) that developmental increases in FNE lead to increased concerns over performance in the presence of peers, which in turn amplifies Hypervigilance for Errors (that is, increased strength of error-related theta oscillations). We further predict (Aim 2) that increased Hypervigilance for Errors leads to more critical self- evaluations and confirmations of initial fears, which worsen FNE/SA over time. Moreover, we predict adolescents who exhibit greater synchrony in theta oscillations across medial-lateral frontal cortex are at greatest risk and will display the largest increases in FNE/SA. To test our model, we will collect an accelerated longitudinal study of 256 adolescents, spanning ages 11-15, biologically male/female, and ranging in FNE/SA. Participants will complete a modified cognitive control task in peer presence/absence (via Zoom) as EEG is recorded. With an eye toward future translational work, we will also (Aim 3) establish the ecological validity of our neural measures by testing links to micro-coded behaviors indicative of SA within a social interaction task. Given that escalation of SA occurs during puberty and within a broader social context, we will also measure, control for, and explore the possible moderating roles of puberty, as well as effects of social and demographic variables. A key strength of this proposal is that our team has a proven record in developmental psychopathology and experimental therapeutics, providing a clear path for translating findings from this project into novel, brain-based therapeutics and thereby shortening the distance “from bench to bedside.”

摘要 社交焦虑症（SAD）是一种慢性的，损害性的疾病，通常出现在青春期， 影响了大约10%的人口SAD的治疗反应率明显低于其他焦虑症 因此，迫切需要确定新的治疗靶点， 治疗这种难以治愈的疾病我们建议通过测试一个发展知情， 在早期到中期的青春期损害社交焦虑症状（SA）的升级机制模型;我们的 模型的核心是对负面评价的恐惧（FNE）和在同伴面前对错误的高度警惕， 重点关注额叶脑振荡，这是这种升级的核心。青春期是一个敏感的时期， 社会认知和认知控制的发展。在心理层面，社交恐惧和FNE表现出 在青少年时期，由于同龄人在这一发展过程中的重要性日益增加， 窗口在神经水平，作为社会认知和认知控制基础的额叶脑系统表现出 青春期的长期发展，包括额叶皮层和相关的4-8 Hz的发展 “theta”振荡与认知控制有因果关系。我们的核心假设是， 在FNE，随着额叶皮层的发展，创造了一个适应不良的反馈回路：青少年成为 对社交环境中的错误高度警惕，进一步增加FNE，最终损害SA。我们的模型预测 (Aim 1）FNE的发展增加导致对存在以下情况下的表现的关注增加： 这反过来又放大了对错误的高度警惕（即，增加了与错误相关的theta强度 振荡）。我们进一步预测（目标2），对错误的过度警惕会导致更多的自我批评， 评估和确认最初的恐惧，随着时间的推移，FNE/SA恶化。此外，我们预测青少年 在内侧-外侧额叶皮层的θ振荡中表现出更大同步性的人风险最大， 将显示FNE/SA的最大增加。为了测试我们的模型，我们将收集一个加速纵向研究， 256名青少年，年龄11-15岁，生物学上为男性/女性，FNE/SA范围不等。参与者将 在记录EEG时，在同伴在场/不在场（通过Zoom）的情况下完成修改的认知控制任务。与 着眼于未来的转化工作，我们还将（目标3）建立我们的神经措施的生态有效性 通过测试指向社交互动任务内的SA的微编码行为的链接。鉴于事态升级 SA发生在青春期和更广泛的社会背景下，我们还将测量，控制和探索 青春期可能的调节作用，以及社会和人口变量的影响。一个关键优势 我们的团队在发展性精神病理学和实验性精神病理学方面有着良好的记录， 治疗学，为将该项目的发现转化为新的基于大脑的治疗方法提供了一条明确的道路 从而缩短“从工作台到床边”的距离。